vitamin a deficiency hypervitaminosis a
DESCRIPTION
VITAMIN A DEFICIENCY AND HYPERVITAMINOSIS A Vitamin A deficiency (VAD) is a major nutritional concern in poor societies, especially in lower income countries like INDIA. Vitamin A is an essential nutrient needed in small amounts for the normal functioning of the visual system, and maintenance of cell function for growth, epithelial integrity, red blood cell production, immunity and reproduction.TRANSCRIPT
VITAMIN A DEFICIENCYAND
HYPERVITAMINOSIS A
Presented by Dr. PANKAJ
Introduction
Vitamin A deficiency (VAD) is a major nutritional concern in poor societies, especially in lower income countries like INDIA.
Vitamin A is an essential nutrient needed in small amounts for the normal functioning of the visual system, and maintenance of cell function for growth, epithelial integrity, red blood cell production, immunity and reproduction.
Active forms are retinol, retinaldehyde, and retinoic acid
Plants synthesize the more complex carotenoids which are cleaved to retinol by most animals and stored in the liver as retinyl palmitate
N retinol plasma values: 15-30 mcg/dl in infants & 30-90 mcg/dl in adults
Retinal is the prosthetic group of photosensitive pigment in both rods (rhodopsin) & cones (iodopsin), major difference lies in the nature of protein bound
Needed in lysosomal membrane stability Plays a role in keratinization, cornification, bone
development & cell growth & reproduction
Absorption of Vitamin A
Retinoids Retinyl esters broken down to free retinol in
small intestine - requires bile, digestive enzymes, integration into micelles
Once absorbed, retinyl esters reformed in intestinal cells
90% of retinoids can be absorbed Carotenoids
Absorbed intact, absorption rate much lower Intestinal cells can convert carotenoids to
retinoids
Transport and Storage of Vitamin A
Liver stores 90% of vitamin A in the body
Reserve is adequate for several months
Transported via chylomicrons from intestinal cells to the liver
Transported from the liver to target tissue as retinol via retinol-binding protein, which is bound to transthyretin
Excretion of Vitamin A
Not readily excreted Some lost in urine Kidney disease and aging increase
risk of toxicity because excretion is impaired
Functions of vitamin A
Vision (night, day, colour) Epithelial cell integrity against
infections Immune response Haematopoiesis Skeletal growth Fertility (male and female) Embryogenesis
Functions of Vitamin A: Growth and Differentiation of Cells
• Retinoic acid is necessary for cellular differentiation
• Important for embryo development, gene expression
• Retinoic acid influences production, structure, and function of epithelial cells that line the outside (skin) and external passages (mucus forming cells) within the body
Functions of Vitamin A: Immunity
Deficiency leads to decreased resistance to infections
Supplementation may decrease severity of infections in deficient person
Prevention of cardiovascular disease Antioxidant capabilities ≥5 servings/day of fruits and vegetables
Cancer prevention Antioxidant capabilities Lung, oral, and prostate cancers Studies indicate that vitamin A-containing foods
are more protective than supplements
Age-related macular degeneration
Cataracts Acne AML
Source of vitamin A
Colostrum foods containing either preformed
vitamin A esters - liver, milk,cheese,eggs or food
products fortified with vitamin A or carotenoid precursors (mainly beta-
carotene), such as green leaves, carrots, ripe mangoes,eggs, and other orange-yellow vegetables and fruits.
Source of vitamin A fruit carotenoid
sources(micrograms/100gm)
Mango (golden) 307 Papaya (solo) 124 Cucurbita (mature pulp) 862 Buriti palm (pulp) 3,000 Red palm oil 30,000 Carrot 2,000 Dark green leafy vegetables
685 Tomato 100 Apricot 250 Sweet potato, red and yellow
670
Animal (micrograms/100gm)
Fatty fish liver oils Halibut 900,000 Cod 18,000 Shark 180,000
Dairy produce Butter 830 Margarine, vitaminized 900 Eggs 140 Milk 40 Cheese, fatty type 320 Liver of sheep and ox 15,000 Beef, mutton, pork 0–4
Units of measuring vitamin A
Each μg RAE corresponds to 1 μg retinol, 2 μg of β-carotene in oil, 12 μg of "dietary" beta-carotene, One International Unit (I.U.) = 0.3 mcg. of retinol = 0.6 mcg. of beta-carotene = 1.2 mcg. of other total mixed
carotenoids
Prevalence of vitamin A deficiency in South Asia (%)
Country sub clinical clinical
VAD (%) VAD (%) Afghanistan 53 - Bangladesh 28 0.7 Bhutan 32 0.7 INDIA 57 0.7 Nepal 33 1 Pakistan 35
High risk group Infancy Childhood Pregnancy Lactation Urban poor Older adults Alcoholism Liver disease (limits storage) Fat malabsorption Increased excretion as in cancer & UTI Low protein intake resulting in deficient carriers
Usually, VAD develops in an environment of ecological social and economical deprivation
Synergism between deficient dietary intake of vitamin A coexists with severe infections, such as measles, and frequent infections causing diarrhoea and respiratory diseases that can lower intake through depressed appetite and absorption, and deplete body stores of vitamin A through excessive metabolism and excretion
Health consequences
Xerophthalmia is the most specific VADD,and is the leading preventable cause of blindness in children throughout the world
Night blindness Anaemia can result from VAD in
children and women,likely due to multiple apparent roles of vitamin A in supporting iron mobilization and transport, and hematopoiesis
Assessing vitamin A status and deficiency
Two sets of indicators of VAD are commonly used for population surveys:
1 clinically assessed eye signs. Term xerophthalmia encompasses the clinical spectrum of ocular manifestations of VAD, from milder stages of night blindness and Bitot’s spots, to potentially blinding stages of corneal xerosis, ulceration and necrosis (keratomalacia)
2 biochemically determined concentrations of retinol in plasma or serum
Classification of xerophthalmia
XNN ight blindness X1A Conjunctival xerosis X1BB itot’s spot X2 Corneal xerosis X3A Corneal ulceration/keratomalacia (<
1/3 corneal surface) X3BCorneal ulceration/keratomalacia (≥
1/3 corneal surface) XSCorneal scar XFXerophthalmic fundus
Serum retinol concentrations
serum retinol concentrations in a population constitutes the second major approach to assessing vitamin
A status in a population, with values below a cut-off of 0.70 μmol/l representing VAD , and below 0.35 μmol/l representing severe VAD.
a serum retinol concentration below a cutoff of 1.05 μmol/l has been proposed to reflect low vitamin.
Criteria for assessing the publichealth significance of xerophthalmia
Clinical (primary) Night blindness (XN)* 1.0% Bitot’s spot (X1B) 0.5% Corneal xerosis and/or
ulceration/keratomalacia (X2 + X3A + X3B) 0.01%
Xerophthalmia-related corneal scars (XS) 0.05%
Biochemical (supportive) Serum retinol (vitaminA) < 0.35 μmol/L (10
μg/dL) 5.0%
Universal vitamin A distribution schedule for preschool and lactating mothers
Children 1–6 years 200,000 IU of vitaminA orally every 3–6
months. Infants 6–11 months 100,000 IU of vitaminA orally every 3–6
months. Lactating mothers 200,000 IU of vitaminA orally once: at
delivery or during the first 8 weeks postpartum if breastfeeding or during the first 6 weeks if not breast-feeding
Recommended xerophthalmia treatment schedule
6 -12 months > 1 yr Immediately 100,000 IU 200,000 IU Next day 100,000 IU 200,000 lU 2–4 weeks later 100,000 IU 200,000 IU
Severe Protein-Energy Malnutrition (PEM) Monthly until PEM resolves 100,000 IU 200,000 IU
Upper Level for Vitamin A
3000 μg retinol Hypervitaminosis A results from long-
term supplement use (2 – 4 x RDA) Toxicity Fatal dose (12 g)
Hypervitaminosis A
Acute Intoxication: Results when excessively large
single doses >300,000 IU ingested Infants: n/v, drowsiness or irritability
w/signs of increased ICP Adults: drowsiness, irritability,
headache & vomiting Serum vitamin A values = 200-1000
IU/dl (N: 50-100 IU/dl)
Toxicity of Vitamin A
Acute – short-term megadose (100 x RDA); symptoms disappear when intake stops GI effects Headaches Blurred vision Poor muscle coordination
Chronic Intoxication Results when >50,000 IU/day ingested for
several wks or more Signs & symptoms in infants:
Early are anorexia, pruritus, irritability, tender swollen bones w/motion limitation
Alopecia, seborrhea, cheilosis & peeling of palms & soles
Hepatomegaly & hypercalcemia observed Craniotabes & hyperostosis of long bones
Elevated serum vit A levels confirms diagnosis
Reversible manifestations when vitamin A discontinued
Chronic Toxicity of Vitamin A
long-term megadose; possible permanent damage Bone and muscle pain Loss of appetite Skin disorders Headache Dry skin Hair loss Increased liver size Vomiting
Toxicity of Vitamin A
Teratogenic (may occur with as little as 3 x RDA of preformed vitamin A) Tends to produce physical defect on
developing fetus as a result of excess vitamin A intake
Spontaneous abortion Birth defects
